The Association between 5HT2A T102C and Behavioral and Psychological Symptoms of Dementia in Alzheimer's Disease: A Meta-Analysis. (16th November 2017)

• Record Type: Journal Article
• Authors: Tang, Liang; Wang, Yan; Chen, Yiwei; Chen, Lianghui; Zheng, Shui; Bao, Meihua; Xiang, Ju; Luo, Huaiqing; Li, Jianming; Li, Yungui
• Other Names: Chiu Helen F. K. Academic Editor.
• Is Part Of: BioMed research international. Volume 2017(2017)
• Publication Date: 2017-11-16
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2017/5320135
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : The serotonin receptor gene (5-HT2A) has been reported to be a susceptible factor in behavioral and psychological symptoms of dementia (BPSD) in Alzheimer's disease (AD). However, previous results were conflicting. We aim to investigate the association of 5-HT2A T102C with BPSD in AD using a meta-analysis. Studies were collected using PubMed, Web of Science, the Cochrane Library databases, Chinese National Knowledge Infrastructure (CNKI), and Embase. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess associations. Nine studies with 1899 AD patients with/without BPSD were included in this meta-analysis. The 102C and CC genotypes were associated with psychosis in AD (102C: p < 0.00001, OR [95% CI] = 3.19 [2.12–4.79]; CC: p < 0.00001, OR [95% CI] = 7.24 [3.60–14.59]). The TT genotype was significantly associated with hallucinations, aberrant motor behavior, and psychosis in AD (hallucinations: p = 0.001, OR [95% CI] = 0.52 [0.36–0.77]; aberrant motor behavior: p = 0.03, OR [95% CI] = 0.58 [0.35–0.95]; and psychosis: p = 0.002, OR [95% CI] = 0.34 [0.17–0.67]). No association was observed between T102C alleles or genotypes and delusions, agitation/aggression, depression, and apathy (p > 0.05 ). Thus, the 5HT2A T102C might be a susceptible factor for hallucinations, aberrant motor behavior, and psychosis in AD. The potential mechanism of this polymorphism in BPSD in AD requires further exploration.